CONCLUSION: "Our results demonstrate a relationship between vitamin D and otolin-1. The majority of our subjects had abnormally low vitamin D levels, but only those over 70 years of age showed a negative correlation with high otolin-1 levels. We postulate that a seasonal drop in vitamin D may not be sufficient for otoconia fragmentation and ultimately iBPPV, rather, chronically low vitamin D maybe required to induce otoconia degeneration."
DOI: 10.1097/MAO.0000000000001747

Previous studies have demonstrated an association of osteopenia/osteoporosis with idiopathic benign paroxysmal positional vertigo (BPPV). Since vitamin D takes part in the regulation of calcium and phosphorus found in the body and plays an important role in maintaining proper bone structure, decreased bone mineral density in patients with BPPV may be related to decreased serum vitamin D. We measured the serum levels of 25-hydroxyvitamin D in 100 patients (63 women and 37 men, mean age ± SD = 61.8 ± 11.6) with idiopathic BPPV and compared the data with those of 192 controls (101 women and 91 men, mean age ± SD = 60.3 ± 11.3) who had lived in the same community without dizziness or imbalance during the preceding year. The selection of the controls and acquisition of clinical information were done using the data from the Fourth Korean National Health and Nutrition Examination Survey, 2008.
The serum level of 25-hydroxyvitamin D was lower in the patients with BPPV than in the controls (mean ± SD = 14.4 ± 8.4 versus 19.1 ± 6.8 ng/ml, p = 0.001). Furthermore, patients with BPPV showed a higher prevalence of decreased serum vitamin D (<20 ng/ml, 80.0 vs. 60.1 %, p < 0.001) than the controls.

Trail lasted only 8 weeks
Can anticipate much better results if the trial had lasted for 12-16 weeks
Note: Since the average got to 34 ng, we can anticipate that about 40% < 30 ng level of vitamin D
Typically little benefit from vitamin D if < 30 ng

BACKGROUND: Benign paroxysmal positional vertigo (BPPV) is a condition with recurrent attacks in a significant proportion of patients. The present case- control study was conducted to assess the influence of serum vitamin D normalization on recurrent attacks of vitamin D deficient patients.

METHODS: Diagnosis of BPPV was made based on history and clinical examination and exclusion of other conditions. Serum 25-hydroxy vitamin D (25-OHD) was measured using ELISA method and a levels of < 20 ng/ml was considered a deficiency of vitamin D. Inclusion criteria were as follows: history of recurrent attacks and serum 25-OHD<20.ng/ml. While the patients with history of trauma, surgery and chronic systemic diseases were excluded. The patients were classified into two groups: treatment and control, intermittently. Both groups received Epley rehabilitation therapy one session per week for 4 weeks but the treatment group received an additional supplement of 50.000 IU of vitamin D (cholecalciferol) weekly for two months to achieve serum 25-OHD ≥ 30 ng/ml and the study patients were followed-up for 6 months.

RESULTS: Twenty-seven patients were allocated to each group. At baseline, serum 25-OHD was similar (10.7±2.3 vs 11.41±1.9, P=0.23). At month 2, serum 25-OHD in the treatment group increased significantly to ≥ 30 ng/ ml, whereas serum 25-OHD in the control group remained unchanged (34.2±3.3 vs 10.6 10.6±2.2 ng/ml, P=0.001). During the follow-up period, attacks of BPPV in the treatment group decreased significantly compared with the control group (14.8% vs 96.3% OR= 0.18, P=0.001).

CONCLUSION: The findings of this study indicate that the normalization of serum vitamin D significantly reduces BPPV recurrences.

BPPV much more common with low vitamin D - Oct 2016

OBJECTIVES: The objective of the present study was to examine the effects of serum 25-hydroxyvitamin D concentrations on patients diagnosed with benign paroxysmal positional vertigo (BPPV) on BPPV recurrence.

STUDY DESIGN: Case series.

METHODS: A retrospective review of 232 patients diagnosed with BPPV visiting the clinic between June 2014 and June 2015 was performed. All patients underwent a complete otolaryngological, audiologic, and neurologic evaluation. The appropriate particle-repositioning maneuver was performed depending on the type of BPPV. The patients were divided into the recurrence group and the nonrecurrence group. Age, gender, follow-up period, type of BPPV, and vitamin D concentrations in the two groups were compared and analyzed through binary logistic regression analyses.

RESULTS: The average follow-up period after treatment was 10.2 months. Forty-one (17.7%) of 232 patients suffered a recurrence during the follow-up period. The mean vitamin D concentration of 191 patients who did not suffer any recurrence was 16.63 ng/mL, whereas that of 41 patients who suffered a recurrence was 13.64 ng/mL. This difference in vitamin D concentrations was statistically significant (P < 0.019). The patients' age, gender, follow-up period, and type of BPPV had no statistically significant impact.

CONCLUSION: Vitamin D is assumed to affect BPPV as a recurrence factor independent of age, gender, follow-up period, and type of BPPV.

Possible reasons for association - clipped from PDF"The authors (of another study) presented two mechanisms of the relationships between BPPV and osteopenia or osteopenia

First, the decrease of estrogen in reducing the natural regulators of bone mass might disturb the internal structure of the otoconia and/or their interconnection and attachment to the gelatinous matrix.

Second, an increase of calcium resorption might generate increased concentration of free calcium in the endolymph and reduce its capacity to dissolve the dislodged otoconia."

See also web

VITAMIN D DEFICIENCY SYMPTOMS & VERTIGO LiveStrong July 2012
Vitamin D deficiency and low calcium levels in the ear can lead to inner ear dysfunction that includes hearing loss, tinnitus or vertigo
Your inner ear is partly responsible for your sense of balance, so ear problems may cause dizziness.
Because vitamin D is necessary for calcium absorption, vitamin D deficiency can lead to osteoporosis and calcium loss in the bones of the inner ear